Implantable medical devices, particularly pacemakers and implantable cardioverter defibrillators (ICDs), are typically configured to be used in conjunction with an external programmer that enables a physician to program the operation of an implanted device to, for example, control the specific parameters by which the pacemaker detects arrhythmia conditions and responds thereto. For instance, the physician may specify the sensitivity with which the pacemaker or ICD senses electrical signals within the heart and also specify the amount of electrical energy to be employed in pacing pulses or defibrillation shocks. Other common control parameters include AV pacing delay values, which for dual chamber devices specify time delays between events sensed in the atria and pacing pulses to be delivered to the ventricles and/or time delays between atrial pacing pulses and ventricular pacing pulses. Additionally, the external programmer may be configured to receive and display a wide variety of diagnostic information detected by the implantable device, such as IEGM signals sensed by the device, as well as diagnostic data from other sources, such as surface electrocardiogram (EKG) systems.
For many patients, particularly those with congestive heart failure (CHF), it is desirable to identify a set of control parameters that will yield optimal cardiac performance (also referred to as hemodynamic performance). Cardiac performance is a measure of the overall effectiveness of the cardiac system of a patient and is typically represented in terms of stroke volume or cardiac output. Stroke volume is the amount of blood ejected from the left ventricle during systole in a forward direction. Cardiac output is the volume of blood pumped by the left ventricle per minute (or stroke volume times the heart rate). In view of the importance of maintaining optimal cardiac performance, especially for patients with compromised cardiac function, it would be desirable to provide improved techniques for use with pacemakers or ICDs for identifying pacing control parameters that optimize cardiac performance, particularly to reduce the degree of heart failure and valvular regurgitation. It is to this end that aspects of the invention are generally directed.
It is particularly desirable to identify AV pacing delay values that provide the best cardiac performance for a particular patient. In normal patients, the electrical conduction through the AV node is intact, and the body automatically adjusts the delay via the circulating hormones and the autonomic nervous system according to its physiologic state. It is well known, for example, that in normal patients, the intrinsic AV delay shortens with increasing heart rate associated with a physiologic stress such as exercise. For patients with abnormal AV node conduction or complete heart block, a pacemaker can control the AV pacing delay by delivering a ventricular pacing pulse at a software-controlled delay after an atrial pulse or intrinsic atrial depolarization. Since the optimum AV delay values vary from person to person, these parameters should be optimized on an individual basis.
Conventionally, the physician attempts to program the AV pacing delay for a given patient by using an external programmer to control the device implanted within the patient to cycle through a set of different AV pacing delay values. For each value, the implanted device paces the heart of the patient for at least a few minutes to permit hemodynamic equilibration, then the physician records a measure of the resulting cardiac performance obtained, for example, using Doppler echocardiography. The AV pacing delay that yields the best cardiac performance is then selected and programmed into the device. However, this is a time consuming and potentially expensive procedure. As a result, some physicians do not bother to optimize the AV pacing delay in many of their patients. Rather, the AV pacing delay is merely set to a default value and is adjusted only if the patient does not respond well to pacing therapy. Hence, many patients are not paced at their particular optimal AV pacing delay value and thus do not obtain the maximal potential benefit from the improved cardiac performance that could otherwise be gained. Moreover, even in circumstances wherein AV pacing delay is optimized by the physician using, for example, Doppler echocardiography, the time and associated costs are significant. In addition, the optimal AV pacing delay for a particular patient may change with time due to, for example, progression or regression in CHF, changes in medications, and/or changes in overall fitness. However, with conventional optimization techniques, the AV pacing delay is re-optimized, if at all, only during specially scheduled follow-up sessions with the physician to allow access to the noninvasive testing equipment such as Doppler-echocardiography, which may be months or perhaps years apart. In addition, separate AV pacing delay values are typically not obtained for use with paced or sensed atrial events. Usually, PV delay is set to be shorter than AV delay when programming either PV or AV delay.
Recently, optimization techniques have been proposed that do not require Doppler-echocardiography but instead use only the surface EKG. See, Strohmer et al., “Evaluation of Atrial Conduction Time at Various Sites of Right Atrial Pacing and Influence on Atrioventricular Delay Optimization by Surface Electrocardiography,” PACE, Vol. 27, April 2004, pp 468-474. Strohmer et al. propose that the AV pacing delay be set based on a surface EKG so as to achieve a 100 millisecond (ms) delay between the end of the P-wave and the peak of the R-wave of the surface EKG. Although an EKG-based technique, such as that of Strohmer et al. eliminates the need to employ Doppler-echocardiography it would instead be desirable to provide techniques that can be performed using IEGM data so that the optimization may be performed by the device itself allowing the AV pacing delay to be automatically and frequently updated in response to change within the patient.
One technique that utilizes IEGM data is set forth in U.S. patent application Ser. No. 10/928,586 of Bruhns et al. filed Aug. 27, 2004, entitled “System and Method for Determining Optimal Atrioventricular Delay Based on Intrinsic Conduction Delays.” Briefly, with the technique of Bruhns et al. intrinsic inter-atrial conduction delays and intrinsic AV conduction delays are determined for the patient and then optimal AV pacing delays are derived therefrom. In one example, the technique uses only IEGM signals and hence can be performed by the device itself without the use of a surface EKG. This permits optimal AV pacing delays to be frequently and automatically updated so as to respond to changes within the patient. In another example, a surface EKG is used to aid in the determination of the inter-atrial conduction delay. In either case, Doppler-echocardiography is not required. The patent application of Bruhns et al. is assigned to the assignee of the present invention and is fully incorporated by reference herein.
Another technique that utilizes IEGM data is set forth in Yu et al., Europace Supplements, Vol. 4, December 2003: A30-6: “Optimization of AV Delay in DDD Mode of Cardiac Resynchronization Therapy for Heart Failure Patients.” With the technique of Yu et al., the AV pacing delay be set to equal to 0.7 (AS−VS)−55 milliseconds (ms), where AS−VS represents the intrinsic AV delay, i.e. the delay between an intrinsic atrial depolarization and an intrinsic ventricular depolarization. Although this allows the AV pacing delay to be set automatically by the implanted device, it is not believed that the formula reliably provides the optimal delay value for many patients. In particular, it does not necessarily achieve a 100 ms delay between the end of the P-wave and the peak of the R-wave, which appears to be optimal. In addition, it does not provide for separate determination of optimal delay values for paced and sensed events.
Accordingly, it would be highly desirable to provide IEGM-based AV pacing delay optimization techniques, which substantially achieve the aforementioned 100 ms delay between the end of a P-wave and the peak of the R-wave for use with either paced or sensed atrial events, but which do not require the use of a surface EKG or require one only during an initial calibration step. It is to this end that the invention is directed.
In terms of nomenclature and abbreviations used herein, “A” is generally used to refer to atrial events, whether paced or sensed, occurring within internal electrical cardiac signals such as an IEGM. “V” is used to generally refer to ventricular events, whether paced or sensed, occurring within the internal electrical cardiac signal. In circumstances where it is necessary to distinguish between paced and sensed events, an “S” or “P” is appended. Hence, AS refers to a sensed atrial event, whereas AP refers to paced atrial event. VS refers to a sensed ventricular event, whereas VP refers to a paced ventricular event. A−V represents the delay between either a paced or sensed atrial event and a paced ventricular event. As already noted, “AV” is simply an abbreviation for “atrioventricular” and should not be confused with A−V, which represents a time delay value.
In circumstances where it is necessary to identify a specific point within an event, such as its beginning, peak or end, an appropriate subscript is also added. As examples, ASEND represents the end of a sensed atrial event and VPPEAK represents the peak of a paced ventricular event. Herein, “peak” refers to the peak of the absolute value of a signal. Depending upon signal polarity, the peak may be positive or negative (i.e. a nadir.) Sensed events are also referred to herein as depolarizations as they are representative of electrical depolarization of myocardial tissue. Paced events are also referred to herein as evoked responses. Paced events in the atria are triggered by APULSES, which are electrical pacing pulses delivered by the implanted device to the atria. Paced events in the ventricles are triggered by VPULSES, which are electrical pacing pulses delivered by the implanted device to the ventricles. The delay between an APULSE and a VPULSE is referred to herein as APULSE−VPULSE and should not be confused with AP−VP, which instead represents the delay between an atrial evoked response triggered by an APULSE and a ventricular evoked response triggered by a VPULSE. Similarly, AS−VPULSE represents the time delay between an intrinsic atrial depolarization and a VPULSE and should not be confused with AS−VP, which instead represents the delay between the atrial depolarization and the ventricular evoked response. APULSE−VPULSE and AS−VPULSE correspond to the aforementioned AV pacing delay values for paced and sensed atrial events. In circumstances where it is desirable to identify an “initial” delay value or a “preferred” delay value, appropriate superscripts are employed, such as AS−VPULSEINITIAL or APULSE−VPULSEPREFERRED, where AS−VPULSEPREFERRED specifies an initial value of the AS−VPULSE delay and APULSE−VPULSEPREFERRED specifies a preferred value for the APULSE−VPULSE delay. Where appropriate, an “L” or “R” subscript may be employed to distinguish between the left and right chambers of the heart. For example, APR refers to a paced event in the right atrium. VSR refers to a sensed event in the right ventricle.
The term “intrinsic delay,” as used herein, refers to the delay between a paced or sensed event in one chamber and a subsequent depolarization in another chamber. For example, an “intrinsic AV delay” refers to the delay between a paced or sensed atrial event and a subsequent sensed ventricular event, e.g. an AS−VS or AP−VS delay. Note also that electrical events detected within an internally sensed electrical cardiac signal typically correspond to events detectable within a surface EKG. In this regard, the P-wave of the surface EKG generally corresponds to either an atrial sensed event (AS) or an atrial paced event (AP) with the IEGM; the R-wave of the surface EKG generally corresponds to either a ventricular sensed event (VS) or a ventricular paced event (VP) with the IEGM. The T-wave of the surface EKG generally corresponds to a ventricular repolarization event of the IEGM. The events within the surface EKG, however, may differ from the corresponding events within the IEGM as to both timing and shape.